emergency dermatology dr melissa barkham spotlight seminar 30 th september 2010
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Emergency Dermatology Dr Melissa Barkham Spotlight Seminar 30 th September 2010. Why is this important?. Urgent recognition and treatment of dermatologic emergencies can be life saving and prevent long term morbidity - PowerPoint PPT PresentationTRANSCRIPT
Emergency Dermatology
Dr Melissa Barkham
Spotlight Seminar 30th September 2010
Why is this important?
Urgent recognition and treatment of dermatologic emergencies can be life saving and prevent long term morbidity
How do you differentiate rare life threatening conditions from the common skin complaints that make up 10 - 20% of consultations in primary care?
Skin structure and function
Protective barrier (toxins, microbes, u.v. light, physical injury)
Temperature regulation Fluid homeostasis Sensation Immunological function Synthetic
(e.g. Vitamin D) Psycho-social
Consequences of Skin failure
Similar to patients with extensive burns
DehydrationFluid and electrolyte imbalanceHypo - albuminaemiaHypotensionHypothermiaSepsisOther organ failure (e.g. renal, hepatic, CCF)
Emergency Dermatology Overview
Skin signs a diagnostic clue (to serious underlying disorder)
Severe Infections (e.g. meningococcaemia, necrotising facsiitis, staphylococcal scalded skin)
Acute autoimmune disease(e.g. SLE, systemic vasculitis)
Paraneoplastic(e.g. dermatomyositis)
Skin disease causing risk of vital organ failure / death
Severe adverse drug reactions (e.g. toxic epidermal necrolysis)
Erythroderma(e.g. due to extensive inflammatory skin disease )
Autoimmune Blistering disorders (e.g. pemphigus vulgaris)
Team approach
GP Accident and emergency On call medical
(or paediatric) teamDermatology consultants and
specialist nurses ITU HistopathologyMicrobiology…..to name but a few
Cutaneous Adverse Drug Reactions
Common - severity variableCan be life threatening Potential long term sequelae
(e.g. blindness)Think carefully before you
prescribe any medicine!Yellow card reporting (MHRA)Over the counter drugs and
supplements can be the culprit
Cutaneous Adverse Drug Reactions
History may not be volunteered
Ask about all medications taken in the last 3 months
Prescribed and non prescribed (including household remedies, herbal remedies, vitamins and supplements)
Beware compound preparations (e.g. cold and flu remedies)
Severe Drug reaction - types
Exanthemous (morbilliform) Stevens - Johnson Syndrome
(SJS) and Toxic Epidermal Necrolysis (TEN)
Drug hypersensitivity syndrome (DHS)
Urticaria +/- angioedema
Drug reaction - warning signs
Facial or mucous membrane involvement
Widespread erythemaSkin painBlistering / skin necrosisFeverLymphadenopathy / arthralgiaFeatures of anaphylaxisOther organ involvement
(e.g. hepatic or renal dysfunction)
Exanthemous drug reaction - features
Commonest typeOnset 5-10 days after new drug Morbilliform (measles like)
maculopapular rashUsually itchySometimes associated with fever / malaiseCommoner in patients with infectious
mononucleosis, leukaemia or HIVSuspected drug (or drugs) should be
discontinued and rash subsides in 1-2 weeks
Exanthemous drug eruption - culprits
PenicillinsCarbamazepineAllopurinolSulphonamidesNSAIDSPhenytoin Isoniazid
DHS - clinical features
Morbilliform rash with fever and internal organ involvement
“Toxic erythema”Mortality - about 10%Later onset (2-6 weeks) after new drug
commencedFever, lymphadenopathyEosinophilia (DRESS) in someHepatic / renal failureTreatment: withdrawal of offending
drug(s) and supportive care
DHS - culprits
SulphonamidesDapsoneAnticonvulsantsACE inhibitorsBeta - blockersAllopurinolMinocyclineSSRI
TEN / SJS - clinical features
Rare drug reaction - presents with skin and mucosal loss
Variants of the same condition (differentiated by extent of skin involved - TEN >30%, SJS <10%)
Mortality - 50%Mucous membrane involvement (eyes,
mouth, genitalia) - can scarTender, blistering skin and necrotic
epidermis – areas of denuded skinPositive Nikolsky sign (blisters extend
with skin pressure)
TEN / SJS - culprits
More than 100 drugs reported including ...PenicillinsSulfonamidesNSAIDS (including ibuprofen)Anticonvulsants AllopurinolAntiretrovirals .... and even paracetamolSusceptibility factors -
HIV, genetic susceptibility
TEN / SJS - Differential diagnoses
Erythema Multiforme - self limiting reaction triggered by infections e.g. HSV. Typical target lesions especially on acral sites. May involve mucosae.
Staphylococcal scalded skin syndrome (SSSS) - a localised infection with a toxigenic strain of S. Aureus triggers fever, redness of skin and easily ruptured blisters. Flexures often affected and mucosae uninvolved.
Autoimmune blistering disorders
TEN / SJS - investigations
Skin biopsy for histology and direct immunofluorescence (DIF)
H&E sections - basal or full thickness epidermal keratinocyte necrosis, supepidermal blistering (SSSS - the split is higher)
DIF - negative (rules out autoimmune disease)
TEN / SJS - management
Remove all possible culprit drugsSupportive care in ITU or high
dependency setting (skin failure)Careful fluid and electrolyte balanceAnalgesiaNon - adherent dressings / sheetsOphthalmology input Prevention and treatment of secondary infectionsConsider intravenous immunoglobulinFuture avoidance (including 1st degree relatives)
Drug induced Urticaria
Drug induced urticaria can occur with or without angioedema
Up to 3 weeks after first exposure (or minutes on re-challenge)
Types - Type 1 hypersensitivity (e.g. penicillin) -
can be associated with anaphylaxis Mast cell degranulation on first exposure
(e.g. NSAIDS, opiates) Angioedema without urticaria
(e.g. ACE inhibitors)
Drug Induced Urticaria - culprits
NSAIDSPenicillins CephalosporinsSulphonamidesACE inhibitorsCalcium channel
inhibitorsVaccinations
What is Erythroderma?
Intense and widespread reddening of the skin (more difficult to detect in asian / black skin)
> 90% Body Surface area involement
Often associated with exfoliation (exoliative dermatitis / exfoliative erythroderma)
Often results from exacerbation of a pre-existing skin disorder
Causes of Erythroderma
PsoriasisDermatitisCutaneous T- Cell
lymphomaDrugs
(red man syndrome) IdiopathicParaneoplastic
Erythroderma - management
Identify underlying cause (biopsy)Consider hospital admissionSupportive care (e.g. keep warm,
regular emollients, fluid balance, high protein diet)
Treat underlying disease (e.g. severe psoriasis - methotrexate or other systemics, dermatitis - topical or oral corticosteroids)
Avoid oral corticosteroids in severe psoriasis
Generalised Pustular Psoriasis
Rare form of psoriasis (patient presents with widespread sterile pustules on a background of red and tender skin)
Many have a background of chronic plaque psoriasis
Trigger factors include sudden withdrawal of oral (or potent topical) corticosteroids, infections, irritating topical preparations like tar or dithranol, pregnancy and drugs
Generalised Pustular Psoriasis
Pustule swab (exclude infectious causes)
Consider skin biopsyAdmissionFluid balance and supportive
careBland emollientsMay require systemic therapy
(e.g. oral retinoid such as acitretin, Methotrexate or anti-TNF therapy)
Pemphigus Vulgaris - clinical features
Rare autoimmune blistering disorder
The blisters are intra-epidermal (therefore easily ruptured)
IgG autoantibodies against a desmosomal protein
Usually presents initially with mucosal (oral, genital, conjunctival erosions) - difficulty eating
+/- skin erosions / blisters (and positive Nikolsky sign)
Pemphigus Vulgaris - treatment
Confirm diagnosis with skin biopsy (including direct IF)
Fatal before advent of oral corticosteroids
Likely to require admission for supportive care
Non adherent dressingsHigh dose oral steroids initially
(1 mg/kg/day)Prevention / treatment of infectionAdditional steroid sparing agent
usually needed
Bullous Pemphigoid - clinical features
Autoimmune blistering disorder, commoner in the elderly
Split is at the Basement Membrane zone (deeper than in PV)
Crops of tense fluid filled blisters, often with surrounding erythema
ItchyCan be localised or widespreadOral mucosal involvement less
frequent than PVUsually less severe than PV
Bullous Pemphigoid -treatment
Confirm diagnosis with skin biopsy (including direct and indirect IF)
Biopsy confirmation less probable if patient already on oral corticosteroids
Admission not always necessaryTreatment – usually oral +/- topical
corticosteroids (reducing course commencing around 0.5 mg/kg/day)
Attention to dressingsMay need steroid sparing agent
(e.g. dapsone, azathioprine)
Eczema herpeticum
Herpes simplex infections can be more severe and extensive in patients with underlying skin disease (e.g. eczema)
Systemic antivirals +/- antibiotics needed
May need admission Ophthalmology input if eyelids
involved or eyes feel gritty
Learning points
Pause before you prescribe – is this drug really necessary?
Warning signs in severe drug reaction (e.g. fever, mucosal involvement, blistering, tenderness)
Caution with oral corticosteroids in psoriasis (abrupt withdrawal can precipitate generalised pustular psoriasis)
When you need us.....
On call team (via switchboard on 01932 872000) if admission needed
Call dermatology (particularly if admission avoidable but urgent treatment needed)
SPH 01932 723720 01932 722234 01932 722748
Ashford 01784 884352
…and a happy ending……
Any questions?